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PubMed2003

Linoleic acid and antioxidants protect against DNA damage and apoptosis induced by palmitic acid.

Polyunsaturated fats are the main target for lipid peroxidation and subsequent formation of mutagenic metabolites, but diets high in saturated fats are more strongly associated with adverse health effects. We show that the common saturated fatty acid, palmitic acid, is a potent inducer of DNA damage in an insulin-secreting cell line, and in primary human fibroblasts. Damage is not associated with upregulation of inducible nitric oxide synthase, but is prevented by two different antioxidants, alpha-lipoic acid and 3,3'-methoxysalenMn(III) (EUK134), which also partly prevent palmitic acid-induced apoptosis and growth inhibition. Since mutagenic metabolites can be formed from peroxidation of polyunsaturated fatty acids, co-administration of palmitic and a polyunsaturated fatty acid might be particularly harmful. Palmitic acid-induced DNA damage is instead prevented by linoleic acid, which is acting here as a protective agent against oxidative stress, rather than as a source of mutagenic metabolites. These results illustrate the complexity of the relationship of dietary fat intake to genotoxicity.

Antioxidants↗

PubMed1980

Chemical mechanisms for cytochrome P-450 hydroxylation: evidence for acylation of heme-bound dioxygen.

Using isotopic tracer methods, we have shown that dihydrolipoic acid (2,3-thioctic acid) acylates the distal oxygen of ferrous oxygenated Pseudomonas cytochrome P-450, forming a transient acyl peroxide intermediate that facilitates oxygen-oxygen bond cleavage. Single-turnover studies with 18O2 indicate one oxygen-18 atom incorporated into the carboxylate group of lipoic acid for each oxygen-18 inserted into the substrate, camphor, forming the product, exo-5-hydroxycamphor. Such a branching ratio for label indicates that water is initially released from an unlageled position and illustrates that the general P-450 mixed-function oxidase stoichiometry generates H218O from 18O2 only after multiple-turnover equilibration with the acylating carboxylate oxygen. Formation of an acyl peroxide state is a natural intermediate in peracid, "oxene", or radical mechanisms for methylene carbone oxygenation.

Acylation↗

PubMed2000

Potential carcinogenic and inhibitory activity of compounds isolated from Lilium candidum L.

This paper deals with determination of potential carcinogenic and inhibitory activity of 10 compounds isolated from the ethanolic extract of Lilium candidum L. perfonned by DC polarography. The series of investigated compounds consisted of two spirostanol saponins, two pyroline derivatives, jatropham and its glucoside, flavonol kaempferol, 2-fenylethyl-alpha-L-arabinopyranosyl-(1-->6)-beta-D-glucopyranoside, 2-phenylethylpalmitate and methylsuccinic acid. Carcinogenic, resp. mutagenic activity data for these compounds, with the exception of kaempferol, are not available in scientific literature. All tested compounds were reduced in N,N-dimethylformamide in one or two well defined steps. They also fonned a reversible complex with alpha-lipoic acid, a compound serving as an indicator of carcinogenic activity. The marginal diffuse current values of these complexes served as a criterion of a very low potential carcinogenicity. The inhibitory activity of isolates were studied in the presence of 12-O-tetradecanoylphorbol-13-acetate, a specific tumor promoter for an epidermal carcinogenesis, and in the presence of a polyaromatic substance 7,12-dimetylbenz(a)anthracene known as a carcinogen. The spirostanol saponins possessed the highest inhibitory activity (> 70%) and jatropham (66%). The inhibitory activity of jatropham glucoside was significantly lower (49%). Practically zero inhibitory activity was measured for the 2-phenylethylpalmitate and methylsuccinic acid.

9,10-Dimethyl-1,2-benzanthracene↗

PubMed2006

Lead toxicity part II: the role of free radical damage and the use of antioxidants in the pathology and treatment of lead toxicity.

Lead is an environmentally persistent toxin that causes neurological, hematological, gastrointestinal, reproductive, circulatory, and immunological pathologies. The propensity for lead to catalyze oxidative reactions and generate reactive oxygen species has been demonstrated in multiple studies. These reactive oxygen species (ROS) inhibit the production of sulfhydryl antioxidants, inhibit enzyme reactions impairing heme production, cause inflammation in vascular endothelial cells, damage nucleic acids and inhibit DNA repair, and initiate lipid peroxidation in cellular membranes. These wide-ranging effects of ROS generation have been postulated to be major contributors to lead-exposure related disease. Antioxidants - vitamins B6, C and E, zinc, taurine, N-acetylcysteine, and alpha-lipoic acid, either alone or in conjunction with standard pharmaceutical chelating agents - have been studied in lead-exposed animals. The evidence for their use in lead exposure, alone and in conjunction with chelating agents, is reviewed in this article.

Animals↗

PubMed2005

Role of hypothalamic 5'-AMP-activated protein kinase in the regulation of food intake and energy homeostasis.

Although obesity is an epidemic threat to general health worldwide, an effective treatment has yet to be found. Insights into weight-regulatory pathways will accelerate the identification of new molecular targets for anti-obesity agents. 5'-AMP-activated protein kinase (AMPK) is an enzyme activated during low cellular energy charge. In peripheral tissues, the activation of AMPK influences various metabolic pathways, including glucose uptake, glycolysis, and fatty acid oxidation, all of which help to re-establish a normal cellular energy balance. AMPK is also present in the neurons of the hypothalamus, a critical center in the regulation of energy homeostasis. Recent studies from our group and others have shown that many factors (alpha-lipoic acid, leptin, insulin, ghrelin, glucose, 2-deoxyglucose, etc.) cause an alteration in hypothalamic AMPK activity that mediates effects on feeding behavior. Hypothalamic AMPK also appears to play a role in the central regulation of energy expenditure and peripheral glucose metabolism. These data indicate that hypothalamic AMPK is an important signaling molecule that integrates nutritional and hormonal signals and modulates feeding behavior and energy metabolism.

AMP-Activated Protein Kinases↗

PubMed2000

Monoselenolipoic acid may be an outstanding pharmaceutical antioxidant with direct thioredoxin-like activity.

Owing to the low pKa of its selenohydryl group, reduced monoselenolipoic acid (MSL) can be expected to be a very versatile antioxidant with direct thioredoxin-like activity. Since MSL supports the growth of lipoate-dependent bacteria, it can be anticipated that MSL will be susceptible to reversible reduction by one or more of the enzymes that reduces lipoic acid - thus greatly potentiating MSL's utility as an antioxidant. If it is not metabolized to release toxic free selenide, MSL may have interesting pharmaceutical potential.

Antioxidants↗

PubMed2025

Hologenomic insights into the molecular adaptation of deep-sea coral Bathypathes pseudoalternata.

Deep-sea coral ecosystems support biodiversity and nutrient cycling through interactions with symbionts. However, their molecular mechanisms remain unexplored. Here, hologenomic analyses of Bathypathes pseudoalternata are applied to uncover molecular adaptations underpinning host-symbiont interactions. Genomic evidence reveals that B. pseudoalternata exhibits adaptations in nutrient transport, immune response, and lysosomal digestion, reflecting its genomic adjustments for a stable symbiosis. Candidatus Nitrosopumilus bathypathes (78.43% ± 3.65%) is inferred to oxidize host-derived ammonia to synthesize amino acids and vitamins to provision the host. The presence of CRISPR-Cas and restriction-modification (R-M) systems suggests that Ca. Bathyplasma bathypathes and Ca. Thalassoplasma bathypathes (10.68% ± 2.99%) may protect the host from viral infections. Ca. Bathybacter bathypathes (8.39% ± 1.53%) is hypothesized to synthesize heme, lipoic acid, and glutathione, which serve dual functions as antioxidants and nutrients. These findings collectively provide insights into how the hologenome contributes to the survival of B. pseudoalternata in the extreme environment.

Animals↗

PubMed1999

Modelling cortical cataractogenesis 22: is in vitro reduction of damage in model diabetic rat cataract by taurine due to its antioxidant activity?

The protective effect of taurine in model in vitro diabetic cataract and the mechanism of this effect were investigated in isolated rat lenses. Isolated rat lenses were incubated in medium 199 in elevated glucose (55.6 m m) with taurine (5 m m). Taurine concentrations in the lenses were determined by amino acid analysis. Accumulative leakage of the intracellular enzyme lactate dehydrogenase (LDH) was used to estimate damage to the lens, as previously reported. In the clear lenses, prior to vacuole formation, after 1 or 2 days of incubation, the taurine and amino acids in lenses decreased progressively in concentration. In lenses incubated with 5 m m taurine, the level of taurine was increased towards that of control lenses. In taurine-treated lenses LDH leakage was significantly decreased, and lens clarity was maintained, similarly to that found previously for vitamin C and lipoic acid. To test whether taurine has similar antioxidant activity, we tested its ability to decrease luminol luminescence generated by (1) superoxide from hypoxanthine/xanthine oxidase and (2) peroxide from diluted glucose/glucose oxidase. For either superoxide or peroxide, the luminescence was decreased to zero, as a function of increasing taurine concentration, at 30 m m, approximately the physiological concentration of taurine in the lens. Spin trapping confirmed that taurine scavenged superoxide. This is consistent with a role for taurine as an important antioxidant protecting the lens against oxidative insults. Amino acids also had antioxidant activity in this assay, and as a group, when all activities were summed, their loss also contributed significantly to the antioxidant loss. Taken in conjunction with Wolff and Crabbe's observation of increased free radical generation by glucose auto-oxidation in diabetes, this suggests a push-pull mechanism for increased oxidative stress in diabetic cataract, involving both increased free radicals and decreased radical scavenging antioxidants.

Amino Acids↗

PubMed1988

Resolution and characterization of the glycine-cleavage reaction in pea leaf mitochondria. Properties of the forward reaction catalysed by glycine decarboxylase and serine hydroxymethyltransferase.

High-molecular-mass proteins from pea (Pisum sativum) mitochondrial matrix retained on an XM-300 Diaflo membrane ('matrix extract') exhibited high rates of glycine oxidation in the presence of NAD+ and tetrahydropteroyl-L-glutamic acid (H4 folate) as long as the medium exhibited a low ionic strength. Serine hydroxymethyltransferase (SHMT) (4 x 53 kDa) and the four proteins of the glycine-cleavage system, including a pyridoxal phosphate-containing enzyme ('P-protein'; 2 x 97 kDa), a carrier protein containing covalently bound lipoic acid ('H-protein'; 15.5 kDa), a protein exhibiting lipoamide dehydrogenase activity ('L-protein'; 2 x 61 kDa) and an H4 folate-dependent enzyme ('T-protein'; 45 kDa) have been purified to apparent homogeneity from the matrix extract by using gel filtration, ion-exchange and phenyl-Superose fast protein liquid chromatography. Gel filtration on Sephacryl S-300 in the presence of 50 mM-KCl proved to be the key step in disrupting this complex. During the course of glycine oxidation catalysed by the matrix extract a steady-state equilibrium in the production and utilization of 5,10-methylene-H4 folate was reached, suggesting that glycine cleavage and SHMT are linked together via a soluble pool of H4 folate. The rate of glycine oxidation catalysed by the matrix extract was sensitive to the NADH/NAD+ molar ratios, because NADH competitively inhibited the reaction catalysed by lipoamide dehydrogenase.

Amino Acid Oxidoreductases↗

PubMed1999

Enzymatic methylation of arsenic compounds. VII. Monomethylarsonous acid (MMAIII) is the substrate for MMA methyltransferase of rabbit liver and human hepatocytes.

Inorganic arsenite is methylated by some, but not all, animal species to dimethylarsinic acid (DMA). The monomethyl compound containing arsenic in an oxidation state of +3 has been proposed as an intermediate. Using highly purified arsenic methyltransferase from rabbit liver and the partially purified enzyme from Chang human liver hepatocytes, the activity of methylarsonic acid (MMAV) and methylarsonous acid (MMAIII) as a substrate has been characterized by Michaelis-Menten kinetics. The rabbit liver enzyme has a greater affinity for MMAIII (Km = 0.92 x 10(-5) M) than MMAV (Km = 7.0 x 10(-5) M) since the smaller the Km the greater the affinity. In addition, a dithiol, reduced lipoic acid or dithiothreitol, appears to be more active than GSH in satisfying the thiol requirement of the enzyme. Although investigators have been unable to detect the arsenic methyltransferase in surgically removed human liver, its presence in Chang human hepatocytes now has been established. The Km for MMAIII, 3.04 x 10(-6), using MMAIII methyltransferase from Chang human hepatocytes was not greatly different from that of the rabbit liver enzyme.

Animals↗

PubMed1989

Nutrition research with lactic acid bacteria: a retrospective view.

From the above discussion, it is apparent that one or another of the lactic acid bacteria requires each of the B vitamins required by animals and that assay methods developed during study of nutrition of bacteria and yeasts have played a large role in the initial or independent discovery, isolation, and characterization of vitamins, vitamin derivatives, and functionally similar substances. Clear examples include biotin, biocytin, lipoic acid, nicotinic acid, pantothenic acid, pantetheine, folic acid and tetrahydrofolic acid (and their derivatives), pyridoxal, pyridoxamine, and pyridoxamine phosphate. Improved assay methods that use these organisms also have provided much of the currently available information concerning distribution and stability of the vitamins in natural products, while quantitative inconsistencies between assays, when traced to their origin, have frequently revealed previously unknown metabolic precursors, products, or functions of the vitamins and have provided explanations of the mechanisms by which certain peptide growth factors act. Extension of such studies to organisms that cannot yet be grown in media of known composition should provide additional insights into currently obscure areas of nutrition.

Lactobacillus↗

PubMed1991

Primary biliary cirrhosis: paradigm or paradox for autoimmunity.

Primary biliary cirrhosis has been classified as a model autoimmune disease based on striking defects in immune regulation and the presence of autoantibodies to mitochondria. Until recently the significance and definition of mitochondrial autoreactivity was unknown. Since 1987, there has been a vast improvement in the understanding and definition of the biochemical and molecular target autoantigens. The cloning of complementary DNAs for mitochondrial antigens has led to the identification of three enzymes of the 2-oxo-acid dehydrogenase family as the targets of the autoantibodies to mitochondria in patients with primary biliary cirrhosis. The major reactive autoantigen is the E2 subunit of pyruvate dehydrogenase. Immunodominant sites on pyruvate dehydrogenase E2 (autoepitopes) have been mapped and have been shown to be the site of attachment of the functionally important lipoic acid prosthetic group. The autoepitope for the other enzymes probably occupies an equivalent site on the enzyme. The availability and definition of these mitochondrial autoepitopes have allowed specific questions to be addressed relating to the processing and targeting of these autoantigens as well as further studies on mechanisms of immunopathology. Similarly, the availability of well-defined autoantigens could contribute to the development of valid animal models in addition to the already described reproduction of the biliary ductular lesions by transfer of peripheral blood lymphocytes from patients with primary biliary cirrhosis into severe combined immunodeficient mice. Such models will facilitate specific study of the role of major histocompatibility complex expression and the characterization of T-cell reactivity. Thus, primary biliary cirrhosis is a key example of significant progress in autoimmunity being made by use of recombinant DNA technology.

3-Methyl-2-Oxobutanoate Dehydrogenase (Lipoamide)↗

PubMed1989

Molecular basis of mitochondrial autoreactivity in primary biliary cirrhosis.

Primary biliary cirrhosis (PBC), styled as a model autoimmune disease, has a very close association with antibodies to mitochondrial antigens. The cloning of cDNAs for mitochondrial antigens led to their identification as the three enzymes of the 2-oxo-acid dehydrogenase family which includes pyruvate dehydrogenase (PDH). The autoantigen is associated with the E2 subunit of these enzymes. PDH is the 70-74 kDa antigen previously identified by immunoblotting. An immunodominant site (autoepitope) can be mapped to a sequence of PDH-E2 which is the site of attachment of the functionally important lipoic acid prosthetic group. Here, Ian Mackay and Eric Gershwin discuss how autoantigen identification and epitope mapping has now proceeded further in PBC than in other autoimmune diseases, and will allow access to critically important questions on pathogenesis of PBC in particular and autoimmunity in general.

3-Methyl-2-Oxobutanoate Dehydrogenase (Lipoamide)↗

PubMed1993

Comparative metabolism and structure of BCKD-E2 in primary biliary cirrhosis.

The identification and cloning of the mitochondrial autoantigens in primary biliary cirrhosis (PBC) have provided new clues in disease pathogenesis. The two major autoantigens are the E2 subunits of pyruvate dehydrogenase and branched-chain ketoacid dehydrogenase (BCKD). Interestingly, one of these complexes, BCKD-E2, is already well known to clinical medicine based on its association with genetic mutations in maple syrup urine disease (MSUD). Patients with this disease have an inability to metabolize branched-chain amino acids. In the present study, we have taken advantage of the known sequence of BCKD-E2 from normal humans, and addressed the issue of whether there is an altered autoantigen sequence in hepatocytes of individuals with primary biliary cirrhosis. In particular, we examined both the leader sequence and the B-cell immunodominant epitope, the lipoic acid domain. In addition, because patients with PBC have autoantibodies to the BCKD-E2 complex, we have quantitated plasma levels of alpha-ketoacids potentially affected in maple syrup urine disease. These include pyruvic acid (PY), phenylpyruvic acid (PP), alpha-ketoisocaproic acid (KIC) alpha-ketoisovalerate (KIV) and alpha-keto-beta-methylvaleric acid (KMV). The levels of these alpha-ketoacids were compared in patients with primary sclerosing cholangitis and normal volunteers. The sequence of BCKD-E2 obtained from PBC hepatocytes showed homology with normal BCKD. Further studies of autoantigen structure and sequence are clearly indicated, including those involved in mitochondrial transport and localization. Finally, we noted a statistically significant increase in all plasma alpha-ketoacids except alpha-keto-beta-methylvaleric acid in PBC patients.(ABSTRACT TRUNCATED AT 250 WORDS)

3-Methyl-2-Oxobutanoate Dehydrogenase (Lipoamide)↗

PubMed2001

Heterogeneous response of antimitochondrial autoantibodies and bile duct apical staining monoclonal antibodies to pyruvate dehydrogenase complex E2: the molecule versus the mimic.

The 2-oxo-acid dehydrogenase complexes and, in particular, the E2 component of the pyruvate dehydrogenase complex (PDC) are the target of antimitochondrial antibodies (AMA). More than 95% of primary biliary cirrhosis (PBC) patients have detectable levels of autoantibodies to PDC-E2 and in general these react with a region of the molecule that contains the prosthetic group lipoic acid (LA). LA is vital to the function of the enzyme, although there is conflicting evidence as to whether its presence is required for PDC-E2 recognition by AMA. Some, but not all, monoclonal antibodies (mAbs) to PDC-E2 produce an intense staining pattern at the apical surface of bile duct epithelial cells (BEC) in patients with PBC, and it has been argued that the molecule at the apical surface of PBC bile duct cells is a modified form of PDC-E2 or a cross-reactive molecule, acting as a molecular mimic. Herein, we characterize the epitopes recognized by 4 anti-PDC-E2 mAbs that give apical staining patterns (3 mouse and 1 human). In particular, by using a combination of recombinant antigens, competitive inhibition assays, and a unique peptide-on-bead assay, we determined that these apically staining mAbs recognize 3 or 4 distinct epitopes on PDC-E2. More importantly, this suggests that a portion spanning the entire inner lipoyl domain of PDC-E2 can be found at the BEC apical surface. In addition, competition assays with patient sera and a PDC-E2-specific mAb showed significant epitope overlap with only 1 of the 3 mouse mAbs and showed a differential response to the peptide bound to beads. These findings further highlight the heterogeneous response of patient autoantibodies to the inner lipoyl domain of PDC-E2.

Amino Acid Sequence↗

PubMed2003

Glycated albumin increases oxidative stress, activates NF-kappa B and extracellular signal-regulated kinase (ERK), and stimulates ERK-dependent transforming growth factor-beta 1 production in macrophage RAW cells.

Albumin modified by Amadori glucose adducts has been shown to modulate signal transduction and induce alterations in renal glomerular cells that contribute to the development of diabetic nephropathy. However, the participation of this nonenzymatically glycated protein in the pathobiology of atherosclerotic cardiovascular disease in diabetes has not been established. To probe this issue, we used macrophage RAW cells to assess the effects of glycated albumin on molecular events implicated in the pathogenesis of diabetes-related vascular complications. RAW cells were cultured in medium containing 5.5 mmol/L glucose and glycated or nonglycated albumin, with and without the addition of PD98059, a specific inhibitor of mitogen-activated protein kinase/extracellular signal-regulated kinase (ERK), followed by analysis of phosphorylated ERK and the nuclear translocation of nuclear factor (NF)-kappa B and measurement of cellular content of thiobarbituric acid-reactive substances and the concentration of transforming growth factor (TGF)-beta(1) in the spent medium. We demonstrate, for the first time, that glycated albumin activates RAW cell ERK and promotes ERK-dependent increases in TGF-beta(1) production, oxidative stress, and NF-kappa B activation. Preincubation with the antioxidant alpha-lipoic acid partially prevented the glycated albumin-induced increase in NF-kappa B activation. These findings indicate that Amadori-modified glycated albumin modulates macrophage cell biology independent of high glucose concentration. The effects of glycated albumin on RAW cell molecular mediators and cytokine production may have pathophysiologic significance with respect to the accelerated atherosclerosis that occurs in diabetes.

Animals↗

PubMed2005

Neurodegeneration from mitochondrial insufficiency: nutrients, stem cells, growth factors, and prospects for brain rebuilding using integrative management.

Degenerative brain disorders (neurodegeneration) can be frustrating for both conventional and alternative practitioners. A more comprehensive, integrative approach is urgently needed. One emerging focus for intervention is brain energetics. Specifically, mitochondrial insufficiency contributes to the etiopathology of many such disorders. Electron leakages inherent to mitochondrial energetics generate reactive oxygen free radical species that may place the ultimate limit on lifespan. Exogenous toxins, such as mercury and other environmental contaminants, exacerbate mitochondrial electron leakage, hastening their demise and that of their host cells. Studies of the brain in Alzheimer's and other dementias, Down syndrome, stroke, Parkinson's disease, multiple sclerosis, amyotrophic lateral sclerosis, Huntington's disease, Friedreich's ataxia, aging, and constitutive disorders demonstrate impairments of the mitochondrial citric acid cycle and oxidative phosphorylation (OXPHOS) enzymes. Imaging or metabolic assays frequently reveal energetic insufficiency and depleted energy reserve in brain tissue in situ. Orthomolecular nutrients involved in mitochondrial metabolism provide clinical benefit. Among these are the essential minerals and the B vitamin group; vitamins E and K; and the antioxidant and energetic cofactors alpha-lipoic acid (ALA), ubiquinone (coenzyme Q10; CoQ10), and nicotinamide adenine dinucleotide, reduced (NADH). Recent advances in the area of stem cells and growth factors encourage optimism regarding brain regeneration. The trophic nutrients acetyl L-carnitine (ALCAR), glycerophosphocholine (GPC), and phosphatidylserine (PS) provide mitochondrial support and conserve growth factor receptors; all three improved cognition in double-blind trials. The omega-3 fatty acid docosahexaenoic acid (DHA) is enzymatically combined with GPC and PS to form membrane phospholipids for nerve cell expansion. Practical recommendations are presented for integrating these safe and well-tolerated orthomolecular nutrients into a comprehensive dietary supplementation program for brain vitality and productive lifespan.

Aging↗

PubMed2003

Modulation of extracellular homocysteine concentration in human cell lines.

BACKGROUND: Despite the growing evidence that plasma homocysteine is a cardiovascular risk factor, the mechanism behind the vascular injuries is still unknown. Information about the metabolism of homocysteine is, therefore, essential for an understanding of its role in atherogenesis, thereby enabling a modulation of that risk. METHODS: In the present study, we have examined the modulation of extracellular homocysteine in HeLa and hepatoma cell cultures in relation to a changed extracellular thiol redox status and in the presence of specific inhibitors of amino acid transporters. RESULTS: The findings in the present study show that a changed thiol redox status by copper ions, copper chelator or the monothiol, N-acetylcysteine (NAC), affects extracellular homocysteine in the same way in hepatoma cell cultures, but not to the same extent as observed in HeLa cell cultures. However, the dithiols, dithiothreitol (DTT) and alpha-lipoic acid (LA), which lowered extracellular homocysteine concentration in HeLa cell cultures, increased the extracellular total homocysteine concentration in hepatoma cell cultures, probably mainly as a result of increased release of homocysteine extracellularly. Studies with specific inhibitors of amino acid transporters in HeLa cell cultures showed that homocysteine uptake occurred mainly by system A and glutamate transporters. Hepatoma cells seemed to have a much smaller uptake capacity of homocysteine compared to HeLa cells. CONCLUSION: The lack of uptake capacity of homocysteine in hepatoma cells indicates that hepatocytes only play a small role in the elimination of homocysteine from circulation. Intracellular metabolism, cellular export and the complex pattern of homocysteine uptake in different cells are important to examine further in order to possibly be able to lower plasma homocysteine levels.

Acetylcysteine↗